Search

1. The vestibular system responds to accelerations of the head and produces reflex responses that serve a variety of compensatory functions. The neuronal circuitry that mediates vestibulo-respiratory reflexes is largely unknown. The purpose of the present study was to investigate the possible role of bulbospinal inspiratory neurons located in the para-ambigual region of the ventral respiratory group (VRG) in mediating these reflexes. Experiments were carried out in cats that were decerebrated, paralyzed, and artificially ventilated. 2. Activation of the vestibular nerve by electrical stimulation produced prominent bilateral reflex responses recorded from the phrenic nerve, which supplies the diaphragm. The responses could be complex and consisted of a decrease and/or increase in nerve discharge. 3. Extracellular recordings were made from 35 VRG inspiratory neurons that were antidromically activated from the upper cervical spinal cord. Almost one-half of these neurons (15/35, 43%) responded to vestibular stimulation. The neuronal response patterns were consistent with VRG inspiratory neurons contributing to the vestibular reflex response simultaneously recorded from the phrenic nerve. 4. The present results indicate that approximately one-half of VRG bulbospinal inspiratory neurons contribute to vestibulo-respiratory reflexes. These findings are in contrast to our recent neuroanatomic and electrophysiological studies which revealed a paucity of vestibular inputs to the dorsal respiratory group (DRG) located in the ventrolateral nucleus of the solitary tract. Thus there appears to be a difference between inspiratory neurons in the DRG and VRG in regard to participating in vestibulo-respiratory reflexes.

1. An in vitro brain stem slice preparation from adult guinea pigs was used to determine the properties of neurons located in the ventral part of the nucleus tractus solitarius (NTS), an area associated with the dorsal respiratory group. Based upon their morphology and their repetitive firing properties, three classes of ventral NTS neurons, termed types I, II, and III, were observed. 2. Type I neurons were multipolar with pyramidal-shaped cell bodies. These neurons responded to prolonged depolarizations from a resting level of -50 mV with a discrete, high-frequency burst of spikes, which rapidly adapted to a low steady-state level. When depolarized from levels more negative than -65 mV, the initial burst was diminished. 3. Type II neurons were multipolar with fusiform-shaped cell bodies. Type II neurons responded to depolarizations from -50 mV with an initial high spike frequency, which gradually adapted to a steady-state level. When depolarized from levels more negative than -60 mV, these neurons displayed a delay between the onset of the stimulus and the first spike. This delay has been termed “delayed excitation.” The expression of delayed excitation was modulated by both the size and duration of hyperpolarizing prepulses that preceded depolarization. 4. Type III neurons were multipolar with spherical shaped-cell bodies. In response to depolarizations from -50 mV, these neurons displayed high-frequency firing with little adaptation. The repetitive firing properties of type III neurons were not modulated by hyperpolarization. 5. Bulbospinal neurons in the ventral NTS were identified using retrograde transport of rhodamine-labeled latex beads injected into the region of the phrenic motor nucleus at spinal cord levels C4 through C6. Only type I and type II neurons were labeled in the ventral NTS (0.2-1.0 mm rostral to the obex). Both contralateral and ipsilateral projections were observed. Contralaterally, type I and II neurons were evenly distributed. Ipsilaterally, however, type II neurons accounted for two-thirds of the labeled neurons. 6. Type I and II neurons had similar input resistances and time constants: 97.0 +/- 17.6 M omega and 14.4 +/- 2.2 ms (n = 5) for type I and 107.0 +/- 11.2 M omega and 13.7 +/- 1.6 ms for type II (n = 5).(ABSTRACT TRUNCATED AT 400 WORDS)

1. Intracellular recordings were made from 50 dorsal respiratory group (DRG) neurons in the region of the ventrolateral nucleus of the solitary tract in anesthetized, paralyzed cats ventilated with a cycle-triggered pump whose inflation stroke was triggered by the onset of phrenic nerve inspiratory (I) discharge. Activity was recorded simultaneously in the ipsilateral nodose ganglion from sensory cell bodies of slowly adapting pulmonary stretch receptors (PSRs). 2. Respiratory cycle-related membrane potential changes of DRG neurons were recorded. Twenty-six neurons that did not exhibit spikes were classified as I alpha, I beta or pump (P)-cells by comparing their membrane potential trajectories during I in the presence of lung inflation with that observed during I, but with lung inflation withheld. The remaining 24 neurons were classified similarly, but the classification was based upon a comparison of their I-phase spike activity responses with and without lung inflation. I phase-related histograms of either membrane potential or spike activity were constructed to facilitate DRG neuronal classification. Additionally, steady lung inflation of varying magnitudes was applied during the expiratory phase. This prolonged expiration and produced different responses in the neurons. Generally, I beta and P-cells were depolarized, whereas I alpha cells were hyperpolarized. 3. Low-intensity electrical stimulation of the ipsilateral vagus nerve evoked excitatory postsynaptic potentials (EPSPs) in all three DRG neuronal types. P-cells and I beta cells exhibited EPSPs in response to the lowest intensity; generally this intensity was below threshold for the simultaneously recorded PSR. Overall, EPSPs in I alpha cells had the highest thresholds, but some EPSPs could be evoked at thresholds similar to those of the I beta cells. The distributions of the average onset latency of the evoked EPSP overlapped considerably. Thus vagal electrical stimulation cannot be used for unequivocal classification of DRG neurons into I alpha, I beta, and P-cell subpopulations. 4. Using intracellular spike-triggered averaging, single PSRs were shown to generate monosynaptic EPSPs in I beta neurons and P-cells but not I alpha cells. Divergence of single PSR afferents also was observed. Relationships between EPSP shape factors, amplitudes, and PSR afferent conduction velocity are similar to those previously observed for monosynaptic EPSPs in hindlimb motoneurons generated by spinal afferents.

1. The ventral part of the nucleus tractus solitarius in guinea pigs comprises the dorsal respiratory group and is composed of three classes of neurons. These have been termed types I, II, and III. Each cell type possesses a unique set of repetitive firing properties. An in vitro brain stem slice preparation was used to study the ionic basis for these repetitive firing properties. 2. Three different membrane currents were shown to contribute to the repetitive firing properties. These were: a slow calcium current (ICa), an early, transient potassium current (IKA), and a calcium-activated potassium current (IKC). Type I and II neurons displayed physiologically significant amounts of these currents; type III neurons did not. 3. During depolarization from potential levels between -50 and -60 mV, the repetitive firing properties of type I and II neurons were determined primarily by ICa and IKC. IKA was inactivated in this potential range. The expression of IKC was greater in type I neurons than in type II neurons, and as a result, type I neurons exhibited a self-terminating burst of spike activity early in depolarization, whereas type II neurons displayed a gradual decline in spike frequency throughout depolarization. 4. The properties of IKA in type I and II neurons were studied using the single-electrode voltage-clamp technique. The kinetics of IKA in type I neurons was approximately twice as slow as those of type II neurons. In addition, the voltage dependence of activation and the removal of inactivation for IKA in type I neurons were shifted by about -10 mV with respect to type II neurons. 5. Depolarization of type I neurons from membrane potential levels where inactivation of IKA was removed caused a decrease in the frequency of the initial burst of spikes. This decrease in spike frequency was result of the coactivation of IKA with ICa. 6. Depolarization of type II neurons from membrane potentials where inactivation of IKA was removed caused a long delay between the onset of depolarization and the beginning of spike activity. The delay in excitation was modulated by both the magnitude and duration of the prestimulus hyperpolarization. This modulation of delayed excitation paralleled the time and voltage dependence for the removal of IKA inactivation in type II neurons.

In decerebrate paralyzed cats ventilated with a cycle-triggered pump system that delivered inflation during the central inspiratory (I) phase (indicated by efferent phrenic discharge), activity of 90 neurons with inspiratory-modulated discharge was recorded in the region of the ventrolateral nucleus of tractus solitarius (vlNTS) in the medulla. Of these, 82 had centrally originating I patterns (69 augmenting, 13 decrementing), and 8 were "pump" neurons. The neurons were classified into functional types by the application of inflation tests, the main test being withholding of the inflation usually delivered during the central I phase. This maneuver eliminated phasic pulmonary afferent input and produced lengthening of the I phase. The neurons' responses were heterogeneous, and were classified as: excitation by inflation (inflation(+], no significant effect of inflation (inflation(0], and depression by inflation (inflation(-]. Application of inflation during the expiratory (E) phase only rarely produced excitation of central I neurons. The I neurons excited by inflation correspond to the "I-beta" neurons of earlier studies. On the basis of the multimodal distribution of their discharge onset times relative to phrenic onset, they were classified as early onset or late onset. In contrast, the inflation(0) and inflation(-) neurons, which correspond to the "I-alpha" neurons, almost exclusively had early onsets. The pump neurons could be distinguished from the inflation(+) I neurons by the effects of inflations delivered during E: the former were equally excited by inflations during E and during I, while the latter were not excited or were minimally excited by inflation during E. Thus, the pump neurons had lung afferent inputs but no inputs from the central I pattern generator, while the inflation(+) I neurons had both kinds of input. The neurons having decrementing discharge during I (early inspiratory and expiratory-inspiratory) were depressed by inflation. Cross-correlation histograms (CCH) of unit firing versus whole phrenic (contralateral and ipsilateral) activity on a short time scale (milliseconds) were computed; the majority of these had high-frequency oscillations, with mean period of 14.6 +/- 3.6 (SD) ms. The CCHs for the different groups of neurons were analyzed with respect to a) strength of correlation as a function of laterality and b) lag of the main correlation peak. Both the inflation(0) and inflation(+) neuronal groups had correlation properties suggesting that these neurons monosynaptically excite phrenic motoneurons.(ABSTRACT TRUNCATED AT 400 WORDS)